Institution
University of New South Wales
Education•Sydney, New South Wales, Australia•
About: University of New South Wales is a education organization based out in Sydney, New South Wales, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 51197 authors who have published 153634 publications receiving 4880608 citations. The organization is also known as: UNSW & UNSW Australia.
Topics: Population, Poison control, Health care, Mental health, Silicon
Papers published on a yearly basis
Papers
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TL;DR: Current tools, frameworks, and trends that aim to facilitate mashup development are overviewed and a set of characteristic dimensions are used to highlight the strengths and weaknesses of some representative approaches.
Abstract: Web mashups are Web applications developed using contents and services available online. Despite rapidly increasing interest in mashups, comprehensive development tools and frameworks are lacking, and in most cases mashing up a new application implies a significant manual programming effort. This article overviews current tools, frameworks, and trends that aim to facilitate mashup development. The authors use a set of characteristic dimensions to highlight the strengths and weaknesses of some representative approaches.
480 citations
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TL;DR: Two individuals with soma-wide, allele-specific and mosaic hypermethylation of the DNA mismatch repair gene MLH1 are reported, with one having had multiple primary tumors that show mismatch repair deficiency and both meeting clinical criteria for hereditary nonpolyposis colorectal cancer.
Abstract: Epigenetic silencing can mimic genetic mutation by abolishing expression of a gene. We hypothesized that an epimutation could occur in any gene as a germline event that predisposes to disease and looked for examples in tumor suppressor genes in individuals with cancer. Here we report two individuals with soma-wide, allele-specific and mosaic hypermethylation of the DNA mismatch repair gene MLH1. Both individuals lack evidence of genetic mutation in any mismatch repair gene but have had multiple primary tumors that show mismatch repair deficiency, and both meet clinical criteria for hereditary nonpolyposis colorectal cancer. The epimutation was also present in spermatozoa of one of the individuals, indicating a germline defect and the potential for transmission to offspring. Germline epimutation provides a mechanism for phenocopying of genetic disease. The mosaicism and nonmendelian inheritance that are characteristic of epigenetic states could produce patterns of disease risk that resemble those of polygenic or complex traits.
479 citations
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TL;DR: The overall prospects for a range of approaches that can potentially exceed Shockley-Queisser limits are assessed, based on ultimate efficiency prospects, material requirements and developmental outlook.
Abstract: The past five years have seen significant cost reductions in photovoltaics and a correspondingly strong increase in uptake, with photovoltaics now positioned to provide one of the lowest-cost options for future electricity generation. What is becoming clear as the industry develops is that area-related costs, such as costs of encapsulation and field-installation, are increasingly important components of the total costs of photovoltaic electricity generation, with this trend expected to continue. Improved energy-conversion efficiency directly reduces such costs, with increased manufacturing volume likely to drive down the additional costs associated with implementing higher efficiencies. This suggests the industry will evolve beyond the standard single-junction solar cells that currently dominate commercial production, where energy-conversion efficiencies are fundamentally constrained by Shockley-Queisser limits to practical values below 30%. This Review assesses the overall prospects for a range of approaches that can potentially exceed these limits, based on ultimate efficiency prospects, material requirements and developmental outlook.
479 citations
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TL;DR: In this paper, high spatial resolution radio continuum and 6.67 GHz methanol spectral line data are presented for methanhol masers previously detected by Walsh et al. They show that the maser is most likely present before an observable UC Hii region is formed around a massive star and is quickly destroyed as the UC H ii region evolves.
Abstract: High spatial resolution radio continuum and 6.67-GHz methanol spectral line data are presented for methanol masers previously detected by Walsh et al. (1997). Methanol maser and/or radio continuum emission is found in 364 cases towards IRAS-selected regions. For those sources with methanol maser emission, relative positions have been obtained to an accuracy of typically 0.05 arcsec, with absolute positions accurate to around 1 arcsec. Maps of selected sources are provided. The intensity of the maser emission does not seem to depend on the presence of a continuum source. The coincidence of water and methanol maser positions in some regions suggests there is overlap in the requirements for methanol and water maser emission to be observable. However, there is a striking difference between the general proximity of methanol and water masers to both cometary and irregularly shaped ultracompact (UC) H ii regions, indicating that, in other cases, there must be differing environments conducive to stimulating their emission. We show that the methanol maser is most likely present before an observable UC H ii region is formed around a massive star and is quickly destroyed as the UC H ii region evolves. There are 36 out of 97 maser sites that are linearly extended. The hypothesis that the maser emission is found in a circumstellar disc is not inconsistent with these 36 maser sites, but is unlikely. It cannot, however, account for all other maser sites. An alternative model which uses shocks to create the masing spots can more readily reproduce the maser spot distributions.
479 citations
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University of Pennsylvania1, Autonomous University of Barcelona2, Mayo Clinic3, University of Manchester4, Erasmus University Rotterdam5, VU University Amsterdam6, Indiana University – Purdue University Indianapolis7, University of Siena8, National Institutes of Health9, Neuroscience Research Australia10, University of Cambridge11, University of Michigan12, Oregon Health & Science University13, Northwestern University14, King's College London15, University of Texas at Dallas16, University of Texas Southwestern Medical Center17, University of Barcelona18, University of Zurich19, Ludwig Maximilian University of Munich20, Duke University21, University of California, San Francisco22, Boston University23, Veterans Health Administration24, Emory University25, University College London26, University of British Columbia27, University of Pittsburgh28, University of Virginia29, University of Antwerp30, Flanders Institute for Biotechnology31, Columbia University32, Johns Hopkins University33, University of Sydney34, University of New South Wales35, University of Washington36, University of Sheffield37, Washington University in St. Louis38, Alfred Hospital39, University of California, Davis40, Harvard University41, Icahn School of Medicine at Mount Sinai42, Rush University Medical Center43, University of Arizona44, University of California, Los Angeles45, University of Southern California46, University of Eastern Finland47, Uppsala University48, Pierre-and-Marie-Curie University49, University of California, San Diego50, University of California, Irvine51, University of Toronto52, University of Alabama at Birmingham53, University of Würzburg54, Karolinska Institutet55
TL;DR: It is found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM 106B, which implicate variants in TMEM106B as a strong risk factor for FTLD, suggesting an underlying pathogenic mechanism.
Abstract: Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). FTLD-TDP is frequently familial, resulting from mutations in GRN (which encodes progranulin). We assembled an international collaboration to identify susceptibility loci for FTLD-TDP through a genome-wide association study of 515 individuals with FTLD-TDP. We found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM106B. Three SNPs retained genome-wide significance following Bonferroni correction (top SNP rs1990622, P = 1.08 x 10(-11); odds ratio, minor allele (C) 0.61, 95% CI 0.53-0.71). The association replicated in 89 FTLD-TDP cases (rs1990622; P = 2 x 10(-4)). TMEM106B variants may confer risk of FTLD-TDP by increasing TMEM106B expression. TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism.
479 citations
Authors
Showing all 51897 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald C. Kessler | 274 | 1332 | 328983 |
Nicholas G. Martin | 192 | 1770 | 161952 |
John C. Morris | 183 | 1441 | 168413 |
Richard S. Ellis | 169 | 882 | 136011 |
Ian J. Deary | 166 | 1795 | 114161 |
Nicholas J. Talley | 158 | 1571 | 90197 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Bruce D. Walker | 155 | 779 | 86020 |
Xiang Zhang | 154 | 1733 | 117576 |
Ian Smail | 151 | 895 | 83777 |
Rui Zhang | 151 | 2625 | 107917 |
Marvin Johnson | 149 | 1827 | 119520 |
John R. Hodges | 149 | 812 | 82709 |
Amartya Sen | 149 | 689 | 141907 |
J. Fraser Stoddart | 147 | 1239 | 96083 |